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Biomedical subjects

J Infante

Publications and source records attributed to J Infante.

29 records · Page 2Linked to original sources
PubMed2000

[Progressive anarthria: one case without lingual apraxia].

Progressive anarthria is a focal cortical degenerative disorder characterized by a profound, progressive alteration in speech without impairment in other cognitive domains. The first symptoms consist of an alteration in the articulation of speech producing telegraphic speech. The disorder invariably progress towards anarthria by deprogramming of the phonation and orolingual movements (bucophonetic apraxia). This type of apraxia is usually associated with orolinguofacial apraxia and it has been anatomofunctionally correlated with frontal opercular involvement of left predominance. The patient presented as progressive anarthria in the absence of manifest orolingual apraxia associated with a predominance of cortical atrophy in the right frontal operculum. This semiological dissociation emphasizes the importance of bucophonatory apraxia in the pathophysiology of progressive anarthria.

Apraxias↗
PubMed1999

[CEA, CA 19.9 and CA 195 in patients with colorectal carcinoma. ROC analysis].

The aim of this study was to assess the utility of determining serum levels of the CEA, CA 19.9 and CA 195 tumor markers in 906 patients with colorectal carcinoma for a 5-year follow-up period. In addition to calculating sensitivity and specificity for the common normal limits, the results were analyzed with RO curves. Sensitivity values for 90% and 95% specificity were also obtained. The results of the areas under the curve (CEA: 0.887; CA 19.9: 0.802; CA 195: 0.971) and sensitivities and specificities at different normality limits showed better behavior for CEA with respect to CA 19.9 and CA 195, the last two presenting similar results. CEA continues to be the best tumor marker to monitor patients with colorectal carcinoma.

Adenocarcinoma↗
PubMed1998

[Radionuclide bone scanning in patients with breast carcinoma. Study of lesions by stages, locations and diagnostic assessment].

The aim of this study was to evaluate the diagnostic role of bone scan in patients with breast carcinoma. With this purpose, we have studied 591 patients (4 males). In 261 of them, we were able to establish the stage of disease: 33 in stage I, 137 in stage II, 71 in stage III y 20 in stage IV. Metastatic lesions were detected in 6% of patients in stage I, 8.8% in stage II, 12.7% in stage III y 50% in stage IV. Altogether, 71 from 591 patients (12%) had metastatic lesions. In 4 patients (5.3%) we obtained a false positive result. The bone lesions found in the scintigraphic studies were classified as not metastatic lesions in 236 patients (39.9%) but 26 of them were malignant (11%). Another 193 patients (32.6%) presented scintigraphic studies considered as equivocal for metastasis and 33 of them were also malignant (17%). In 150 patients scintigraphic studies did not present lesions during the follow up. In other 156 patients isolated lesions were detected and 24 of them (15.4%) were malignant. Only 4 < > lesions were detected and not any < > image was observed in this study.

Adult↗
PubMed1992

Regulation of HMG-CoA reductase, apoprotein-B and LDL receptor gene expression by the hypocholesterolemic drugs simvastatin and ciprofibrate in Hep G2, human and rat hepatocytes.

The comparative effects of simvastatin (a competitive inhibitor of HMG-CoA reductase) and ciprofibrate (another inhibitor of cholesterogenesis) on the incorporation of [14C]acetate and [3H]mevalonate into cholesterol HMG-CoA reductase activity, apo-B synthesis, LDL receptor, and their corresponding mRNAs, have been studied in the human hepatoma cell line Hep G2 and in human and rat hepatocytes in primary culture. Incubation of Hep G2 with simvastatin (0.01-1.5 microM) or ciprofibrate (25-100 microM) produced not only a marked inhibition of cholesterogenesis from [14C]acetate but also from [3H]mevalonate, an intermediate downstream of the HMG-CoA reductase reaction. However, in human and rat hepatocytes, cultured in similar conditions, simvastatin inhibited only the cholesterol synthesis from [14C]acetate, as expected. HMG-CoA reductase activity was greatly induced in Hep G2 and rat hepatocytes after incubation with simvastatin (up to 400% of controls), but not with ciprofibrate. Increased enzyme activity was accompanied by a higher cell content of reductase mRNA. Apo-B concentration in the medium of Hep G2 cells was 31% lower after 31 h incubation with simvastatin than in controls. However, neither simvastatin nor ciprofibrate modified the synthesis rate of apo-B or its mRNA level. Both LDL-receptor and its mRNA levels were raised by simvastatin at concentrations inhibiting cholesterol synthesis. Our data show that, in this human hepatoma cell line, HMG-CoA reductase competitive inhibition by simvastatin triggers a coordinate regulation of the expression of genes coding for reductase and LDL receptor but not for apo-B. Ciprofibrate, though efficient in inhibiting cholesterogenesis, did not induce the same regulatory reactions. The reason for this discrepancy is unknown.

Acetates↗
PubMed1990

Experimental colorectal liver metastases. Influence of sex, immunological status and liver regeneration.

The liver is the most frequent site of metastases from colon cancer. To improve our knowledge of liver metastases and to develop new adjuvant therapies, a good animal model is necessary. The aims of this study were to obtain a model of liver metastases with intraportal injection of colon adrenocarcinoma cell aggregates (DHDK12 cell line) and to study the effect of various factors, i.e., sex, liver regeneration and immunosuppression, on the development of liver metastasis. Cell aggregates were injected into the portal vein of 59 syngenic male and female BD IX rats following randomization into three groups. Group 1, (control 12 males and 10 females) received only cell aggregates; group 2 (12 males and 10 females) underwent a 70% hepatectomy before cell injection; group 3 (15 males and 10 females) received cyclosporin A injections at a dose of 10 mg/kg per day for 28 days following cell injection. Autopsy was performed at 10 weeks. Liver metastases were more frequent in the male rats in group 3 than in those in group 1 (80% vs. 30%, p less than 0.04). The rate of liver metastases in females was not increased by immunosuppression (22.2% vs. 12.5%, N.S.). Liver resection (group 2) did not significantly modify the incidence of liver metastasis. No female had liver metastases in this group. This relatively simple model rapidly produces liver metastasis with a high yield, but only in male rats. Besides sexual factors, immunosuppression also increased the rate of experimental liver metastasis, while liver regeneration failed to do so.

Adenocarcinoma↗
PubMed1989

Lipid and lipoprotein synthesis in isolated and cultured hepatocytes from lean and obese Zucker rats.

Hepatocytes were isolated by EDTA perfusion of livers from lean (Fa/-) and obese (fa/fa) Zucker rats. Triacylglycerol (TG) and sn-glycerol 3-phosphate were increased in fa/fa hepatocytes, but free fatty acids, cholesterol and phospholipid concentrations were similar in both groups. In spite of an identical fatty acid uptake rate, glycerolipid synthesis was higher in obese compared to lean rat hepatocytes, and this difference remained for at least 2-3 days of culture. Triacylglycerol mass secretion was 2-fold higher in obese than in lean rat hepatocytes. This was confirmed by the higher incorporation of labeled glycerol and oleic acid into the medium TG fraction floating at density 1.006 g/ml. Density gradient ultracentrifugation of [14C]oleate-labeled lipoproteins showed that fa/fa hepatocytes secreted more TG-rich lipoproteins, and that 87% of the label was in the VLDL fraction compared with 67% in the medium of Fa/- hepatocytes. Decreased utilisation of leucine for protein synthesis in obese rat compared to lean rat hepatocytes was associated with enhanced leucine oxidation to CO2. [35S]Methionine incorporation showed an identical cell protein synthesis rate. Autoradiography after PAGE separation of secreted apolipoproteins (apoBh, Bl, apoA-VI, apoE, apoA-I, apoC) showed an identical pattern in both cell types.

Animals↗
PubMed1988

Lipid and lipoprotein metabolism in Hep G2 cells.

Lipid composition, lipid synthesis and lipoprotein secretion by the Hep G2 cell line have been studied with substrate and insulin supplied under different conditions. The lipid composition of Hep G2 cells was close to that of normal human liver, except for a higher content in sphingomyelin (P less than 0.005) and a lower phosphatidylcholine/sphingomyelin ratio. Most of the [14C]triacylglycerols secreted into the medium were recovered by ultracentrifugation at densities of 1.006 to 1.020 g/ml. The main apolipoproteins secreted were apo B-100 and apo A-I. Hep G2 mRNA synthesized in vitro the pro-apolipoproteins A-I and E. Triacylglycerol secretion was 7.38 +/- 1.04 micrograms/mg cell protein per 20 h with 5.5 mM glucose in the medium and increased linearly with glucose concentration. Oleic acid (1 mM) increased the incorporation of [3H]glycerol into the medium and cell triacylglycerols by 251 and 899%, with a concomitant increment in cell triacylglycerols and cholesterol ester. Insulin (1 mU or 7 pmol/ml) inhibited triacylglycerol secretion and [35S]methionine incorporation into secreted protein by 47 and 28%, respectively, with a corresponding increase in the cells. Preincubation of cells with 2.5-10 mM mevalonolactone decreased the incorporation of [14C]acetate into cholesterol 6.2-fold, indicating an inhibitory effect on HMG-CoA reductase. It is concluded that in spite of some differences between Hep G2 and normal human hepatocytes, this line offers an alternative and reliable model for studies on liver lipid metabolism.

Acetates↗
PubMed1985

Isolation of rat hepatocytes with EDTA and their metabolic functions in primary culture.

Isolated hepatocytes from adult rat liver were prepared after dissociation of the liver with EDTA. The morphological appearance, viability (94.5%) and yield (1.76.10(7) cells/g liver) compare well with those of previously described methods using collagenase. Differentiated functions of the hepatocytes in primary culture such as albumin secretion (10.9 micrograms/mg cell protein/d) and triglyceride synthesis and secretion are maintained. Induction of triglyceride synthesis and secretion by oleic acid takes place to an extent similar to that observed in vivo and liver perfusion. Particles with a lipid composition resembling circulating very low density lipoproteins are secreted into the medium. These characteristics demonstrate the ability of hepatocytes isolated with EDTA and subsequently used in primary culture to retain complex and highly differentiated functions of the intact liver.

Albumins↗
PubMed1983

Effects of vitamin E and aspirin on the incidence of encephalomalacia, fatty acid status and serum thromboxane levels in chicks.

This study was initiated to examine the role of prostanoids (thromboxane) in the development of nutritional encephalomalacia (NE). Chicks were fed diets deficient in or supplemented with vitamin E in the presence or absence of a known prostaglandin inhibitor, acetylsalicylic acid (ASA). When the incidence of NE was approximately 50% in the vitamin E--deficient group without ASA supplement, the chicks were killed, and serum thromboxane B2 (TxB2) and serum and brain fatty acid (FA) composition were determined. The incidence of NE was not altered by ASA treatment. Plasma arachidonate levels were increased by ASA treatment on the vitamin E--deficient diet. Furthermore, the serum TxB2 levels in vitamin E--deficient versus vitamin E--adequate chicks, unlike changes noted for rats, were decreased. Aspirin treatment drastically reduced TxB2 levels in all groups but did not alter the incidence of NE. Therefore, it is unlikely that the development of NE is a result of thromboxane-mediated thrombosis.

Animals↗
PubMedDate not supplied

[Endocranial hypertension].

INTRODUCTION AND OBJECTIVE: The endocranial hypertension syndrome is one of the commonest and most feared neurological complications in clinical practice. This encourages its continued study, and is the subject of this review. DEVELOPMENT: Endocranial hypertension is the common pathway for the presentation of many neurological and non neurological disorders. An increase in the volume of one or more intracranial structures causes secondary lesions of the brain and even the death of the patient, although this may frequently be avoided by prompt recognition and suitable action by the doctor involved. General, non specific therapeutic measures should be instituted to achieve a normal endocranial pressure. The clinical presentation and complementary investigations should be correctly interpreted to determine the aetiology of the condition so that specific treatment may be given. Continuous monitoring of the intracranial pressure and other neuromonitorization techniques are essential for correct decisions as to treatment. CONCLUSIONS: Understanding the physiopathology, diagnosis and treatment of the syndrome of endocranial hypertension are still essential in modern medicine. In recent years there have been advances in the use of well known treatments and new drugs have been introduced. Use of the different neuromonitoring techniques permits optimum use of the treatment available.

Brain Edema↗